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Journal of Neuroscience, Vol 12, 1917-1927, Copyright © 1992 by Society for Neuroscience
Prostaglandin E2 increases calcium conductance and stimulates release of substance P in avian sensory neurons
GD Nicol, DK Klingberg and MR Vasko
Department of Pharmacology and Toxicology, School of Medicine, Indiana University, Indianapolis 46202.
Prostaglandins are known to lower activation threshold to thermal,
mechanical, and chemical stimulation in small-diameter sensory neurons.
Although the mechanism of prostaglandin action is unknown, agents known to
elevate intracellular calcium produce a sensitization that is similar to
that produced by prostaglandins. Consistent with the idea of
prostaglandin-induced elevations in calcium, prostaglandins might also
stimulate the release of neurotransmitter from sensory neurons. We
therefore examined whether prostaglandin E2 (PGE2) could enhance the
release of the putative sensory transmitter substance P (SP) from isolated
neurons of the avian dorsal root ganglion grown in culture. Utilizing the
whole-cell patch-clamp recording technique, we also examined whether PGE2
could alter calcium currents in these cells. Exposure of sensory neurons to
PGE2 produced a dose-dependent increase in the release of SP. One
micromolar PGE2 increased release approximately twofold above basal
release, whereas 5 and 10 microM PGE2 increased release by about fourfold.
The release evoked by these higher concentrations of PGE2 was similar in
magnitude to the release induced by 50 mM KCl. Neither arachidonic acid (10
microM), prostaglandin F2 alpha (10 microM), nor the lipoxygenase product
leukotriene B4 (1 microM) significantly altered SP release. The addition of
1 microM PGE2 increased the peak calcium currents by 1.8-fold and 1.4-fold
for neurons held at potentials of -60 and -90 mV, respectively. The action
of PGE2 was rapid with facilitation occurring within 2 min. As with release
studies, arachidonic acid, prostaglandin F2 alpha, and leukotriene B4 had
no significant effect on the amplitude of the calcium current. These
results suggest that PGE2 can stimulate the release of SP through the
activation or facilitation of an inward calcium current. The capacity of
PGE2 to facilitate the calcium current in these sensory neurons may be one
mechanism to account for the ability of prostaglandins to sensitize sensory
neurons to physical or chemical stimuli.
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